Parasitic helminths pose significant health problems throughout the world but, in many cases, adequate means of chemotherapy still are not available. It is clear that many parasitic helminths exhibit a predominantly anaerobic energy metabolism that differs substantially from that of the host and it appears that many potent anthelminthics specifically interfere with helminth energy metabolism. However, much still remains to be elucidated about the energy-generating reactions of the "anaerobic" helminth mitochondrion before the differences between host and parasite can be fully exploited. These organisms do not degrade glucose completely to CO(2) and H(2)0 but, instead, use organic molecules as terminal electron-acceptors and excrete a variety of reduced compounds as end products of carbohydrate degradation. The present study is designed to identify the regulation of branched-chain fatty acid (BFA) synthesis in mitochondria isolated from the procine nematode, Ascaris suum. This organism has served as an excellent model for many studies of helminth metabolism. Volatile branched-chain fatty acids are the major end products of Ascaris mitochondrial metabolism but little is known about the energetics of their formation. In fact, little is known about the overall energy-generating capacity of any helminth mitochondrion. In the present study, the enzyme system catalyzing BFA formation in Ascaris will be purified and characterized and the in vivo source of reducing power for BFA synthesis will be identified. More importantly, studies with intact mitochondria should define the role of electron-transport and possible associated phosphorylation in BFA formation and provide an appreciation for the overall energy-generating capacity of this "anaerobic" mitochondrion. Once the enzymatic differences between host and parasite metabolisms have been evaluated, a more sensible approach to chemotheraphy can be adopted. In addition, the more that is known about the biochemical mode of action of anthelminthics, the more rational efficient drug usage will become.